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Mucosal Defense Against Giardia at the Intestinal Epithelial Cell Interface

Solaymani-Mohammadi, Shahram·2022·Frontiers in Immunology
DOI 10.3389/fimmu.2022.817468PMC PMC8891505
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Abstract

Human giardiasis, caused by the protozoan parasite Giardia duodenalis (syn. Giardia lamblia , Giardia intestinalis , Lamblia intestinalis ), is one of the most commonly-identified parasitic diseases worldwide. Chronic G. duodenalis infections cause a malabsorption syndrome that may lead to failure to thrive and/or stunted growth, especially in children in developing countries. Understanding the parasite/epithelial cell crosstalk at the mucosal surfaces of the small intestine during human giardiasis may provide novel insights into the mechanisms underlying the parasite-induced immunopathology and epithelial tissue damage, leading to malnutrition. Efforts to identify new targets for intervening in the development of intestinal immunopathology and the progression to malnutrition are critical. Translating these findings into a clinical setting will require analysis of these pathways in cells and tissues from humans and clinical trials could be devised to determine whether interfering with unwanted mucosal immune responses developed during human giardiasis provide better therapeutic benefits and clinical outcomes for G. duodenalis infections in humans.

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Figure 1 Giardia infection induces the secretion of AMPs (e.g., defensins, trefoil factors) in parasitized IECs likely via an IL-22/IL-22R-mediated mechanism.
Figure 1 Giardia infection induces the secretion of AMPs (e.g., defensins, trefoil factors) in parasitized IECs likely via an IL-22/IL-22R-mediated mechanism.CC BY · PubMed Central
Figure 2 Schematic model of disaccharidase deficiency following infection with Giardia infection in vivo.
Figure 2 Schematic model of disaccharidase deficiency following infection with Giardia infection in vivo.CC BY · PubMed Central

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Cited by

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Metadata

Authors
Solaymani-Mohammadi, S.
Venue
Frontiers in Immunology
Publisher
Frontiers Media SA
Published
2022-02-17
Volume
13
ISSN
1664-3224
DOI
10.3389/fimmu.2022.817468
PMC
PMC8891505
Cited by
43
References
2
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Institutes of Health
  • University of North Dakota

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